Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the treatment of remitting-relapsing experimental autoimmune encephalomyelitis (EAE) in mice with human bone marrow stromal cells (hBMSCs). hBMSCs were injected intravenously into EAE mice upon onset of paresis. Neurological functional tests were scored daily by grading clinical signs (score 0-5). Immunohistochemistry was performed to measure the transplanted hBMSCs, cell proliferation (bromodeoxyuridine, BrdU), oligodendrocyte progenitor cells (NG2), oligodendrocytes (RIP), and brain-derived neurotrophic factor (BDNF). The maximum clinical score and the average clinical scores were significantly decreased in the hBMSC-transplanted mice compared to the phosphate-buffered-saline-treated EAE controls, indicating a significant improvement in function. Demyelination significantly decreased, and BrdU(+) and BDNF(+) cells significantly increased in the hBMSC-treated mice compared to controls. Some BrdU(+) cells were colocalized with NG2(+) and RIP(+) immunostaining. hBMSCs also significantly reduced the numbers of vessels containing inflammatory cell infiltration. These data indicate that hBMSC treatment improved functional recovery after EAE in mice, possibly, via reducing inflammatory infiltrates and demyelination areas, stimulating oligodendrogenesis, and by elevating BDNF expression.
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PMID:Human bone marrow stromal cell treatment improves neurological functional recovery in EAE mice. 1590 21

The goal of this study was to determine whether oral administration of sodium phosphate in conjunction with intravenous calcium is more efficaceous than intravenous calcium alone for the treatment of parturient paresis. Thirty cows with parturient paresis were examined and treated by the same veterinarian. The cows were divided randomly into two groups of 15 cows each. Cows in group A received 500 ml of a 40 per cent calcium borogluconate solution containing 15.65 g calcium gluconate and borogluconate, with a supplement of 6 per cent magnesium hypophosphite (9.85 g magnesium hypophosphite) intravenously over a period of approximately 15 min. Cows in group B received the same treatment as well as 350 g of monobasic sodium phosphate (70 g inorganic phosphate, NaH2PO4 2 H2O, Streuli) dissolved in 0.5 litres of distilled water orally via a stomach tube. After treatment, the heart rate, respiratory rate, rectal temperature, superficial body temperature, rumen motility, appetite and defecation of the cows were monitored every hour for eight h. The cows' attempts to rise and their ability to stand were also noted. Initially, the results of clinical examination and serum electrolyte analyses did not differ between the two groups of cows. Within one hour of treatment, stupor was not observed in any of the cows. The general demeanour after treatment did not differ significantly between the two groups. In both groups, the average rectal temperature increased within two hours of the initiation of treatment, from 38.0 +/- 0.95 degrees C to 38.5 +/- 0.40 degrees C. There was no significant difference in the recovery rate between the groups. Of the 30 cows, 22 (73.3 per cent) stood within eight hours of treatment (10 cows from group A and 12 cows from group B). The type of treatment did not affect the time required to stand: cows in group A stood within 47.3 +/- 44 minutes and cows in group B stood within 24.2 +/- 32 minutes after the start of treatment. Our findings do not support the hypothesis that oral treatment with 350 g of sodium phosphate together with intravenous infusion of calcium in cows with parturient paresis results in an improved outcome, even though all the cows had hypophosphataemia as well as hypocalcaemia.
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PMID:Effect of intravenous calcium and oral sodium phosphate in cows with parturient paresis. 1764 35

The decrease of the level of serum prostate specific antigen (PSA) after discontinuation of estramustine phosphate (EMP) has rarely been reported. We report 2 cases in whom EMP withdrawal syndrome was encountered. Case 1 was a 68-year-old man with a complaint of paresis of lower limbs. He was diagnosed with prostate cancer with multiple bone metastases. The serum PSA level was 9,300 ng/ml. He was treated with luteinizing hormone-releasing hormone agonist (LH-RHa) and bicalutamide (BCL). Six months later, EMP was started against PSA failure. During the 3-year treatment with EMP, PSA decreased to the nadir of 0.7 ng/ml and gradually increased to 14 ng/ml. After withdrawal of EMP, PSA decreased to 0.3 ng/ml (97.9% decline) and remained at this level for 4 months. Case 2 was a 61-year-old man who visited our hospital with gross hematuria. Transurethral bladder biopsy and transrectal prostate biopsy were performed. The diagnosis was moderately differentiated adenocarcinoma of the prostate that invaded to the bladder. Computed tomography (CT) showed a lymph node metastasis. He was treated with LH-RHa and BCL. The treatment was changed to EMP after PSA failure. EMP was withdrawn when PSA was 30 ng/ml. Then PSA decreased to less than 0.2 ng/ml (99% decline) and remained at this level for 9 months. We consider that in patients with EMP-resistant progression, EMP withdrawal syndrome should be checked.
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PMID:[Estramustine phosphate withdrawal syndrome in relapsed prostate cancer: two case reports]. 1863 39

The goal of this study was to investigate the efficacy of calcium chloride, sodium phosphate or a combination of these two substances administered orally immediately postpartum for the prevention of parturient paresis in cows. Thirty-two cows that had had parturient paresis at the previous calving, and in which serum biochemistry had shown hypocalcaemia and hypophosphataemia, were used in the study. The cows were transferred to the Department of Farm Animals, University of Zurich, five days before their expected due dates. On a randomized trial, the cows were given calcium chloride, sodium phosphate, both substances or no treatment (controls) via a stomach tube immediately postpartum and 12 hours later. The cows were monitored for 96 hours during which time blood was collected on a regular basis for the determination of total calcium, ionized calcium, inorganic phosphorus and magnesium concentrations. Of the 32 cows treated, 19 (59%) had parturient paresis and 13 (41%) did not. The incidence of parturient paresis did not differ significantly among the groups although there was a tendency for a lower incidence in cows treated with both calcium chloride and sodium phosphate. The various treatments had no apparent effect on serum calcium concentration. The concentration of inorganic phosphorus increased significantly in cows treated with sodium phosphate compared with the controls. The results of this study showed that cows treated with both calcium chloride and sodium phosphate orally tended to have a lower incidence of parturient paresis. Further investigation into multiple administrations of oral calcium chloride and sodium phosphate, started before parturition, for the prevention of parturient paresis is required.
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PMID:[Efficacy of oral calcium and/or sodium phosphate in the prevention of parturient paresis in cows]. 1871 36

Thirty cows with parturient paresis were divided into three groups of 10. All the cows were given 500 ml of a 40 per cent calcium borogluconate solution intravenously over a period of 10 minutes, and 20 were also given 500 ml of a 10 per cent solution of sodium phosphate intravenously; in 10 of the cows this solution was administered over a period of 10 minutes immediately after the calcium borogluconate solution, and in the other 10 cows 200 ml of the solution was administered rapidly and the remaining 300 ml was added to 10 litres of sodium chloride and glucose solution and infused slowly over six hours. There were no significant differences between the groups with respect to the outcome of the treatments; six or seven of the cows in each group stood within eight hours of the treatment. There were no significant differences between the changes in serum calcium concentrations among the groups. The mean concentrations of inorganic phosphorus in the groups given sodium phosphate were increased above the normal range initially, but after eight hours there were no significant differences between the groups in terms of the numbers of cows that were hypophosphataemic. There were no significant differences between the three groups with respect to changes after treatment in the serum concentrations of magnesium or parathyroid hormone.
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PMID:Effect of intravenous calcium borogluconate and sodium phosphate in cows with parturient paresis. 1927 Mar 20

This 60-year-old man with cervical spondylosis experienced bilateral arm pain and weakness. After anterior cervical fusion and posterior decompression at a local hospital his symptoms worsened and he was admitted to our hospital. On admission he manifested bilateral motor weakness, neuropathic pain, and numbness below the C5 level. Radiological findings showed spinal cord compression at the C4 to C7 level. He again underwent posterior decompression and anterior fusion. Although his paresis was improved, his severe neuropathic pain and numbness persisted. Because treatment with NSAIDs, clonazepam, and gabapentin failed to control his symptoms we administered ketamine (NMDA receptor antagonist) because his symptoms were alleviated upon ketamine test challenge. His severe symptoms improved and there were no complications. However, upon cessation of ketamine treatment they reappeared. Therefore, we continued daily ketamine treatment for 6 months, after which we changed to codeine phosphate. His symptoms were controlled without any complications. Ketamine is useful for the control of severe neuropathic pain, however, as long-term ketamine administration is inadvisable, we suggest that treatment be tailored to each patient's particular clinical status.
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PMID:[Ketamine treatment for severe neuropathic pain with cervical spondylotic myelopathy. A case report]. 2116 Jan 5

Fifteen cows with milk fever were treated with 500ml of 40 % calcium borogluconate (group A) administered intravenously. Fifteen other cows with milk fever received the same treatment, supplemented with 500ml of 10 % sodium phosphate administered intravenously, and 80g calcium as calcium lactate and 70g inorganic phosphorus as sodium phosphate administered orally in drinking water. The cows were monitored and blood samples collected for 3 days to measure the concentrations of total and ionized calcium, inorganic phosphorus and magnesium and the activity of creatine kinase. The two groups did not differ significantly with respect to the course of the disease. In each group 14 cows were cured. A rapid and significant increase in serum calcium concentration from the hypo- to the hypercalcaemic range occurred in both groups within 10min of the start of treatment, followed by a slow and steady decrease to the hypocalcaemic range. Calcium lactate did not prevent the calcium concentration from returning to the hypocalcaemic range, and the calcium profiles of the two groups did not differ significantly. As expected, treatment had little effect on the concentration of inorganic phosphorus in group A. In group B, treatment caused a rapid increase in the concentration of inorganic phosphorus to a maximum 20min after the start of treatment. This was followed by a slow decrease in the phosphorus concentration to the normophosphataemic range. Our findings confirmed that combined intravenous and oral administration of sodium phosphate in cows with periparturient paresis attributable to hypocalcaemia and hypophosphataemia results in a rapid and sustained increase in serum phosphorus, but not in serum calcium concentration. This modified therapy did not improve the success rate of milk fever treatment and further studies are needed to improve treatment of periparturient paresis.
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PMID:Treatment of cows with milk fever using intravenous and oral calcium and phosphorus. 2292 22

Hypophosphatemia (HP) with or without intracellular depletion of inorganic phosphate (Pi) and adenosine triphosphate has been associated with central and peripheral nervous system complications and can be observed in various diseases and conditions related to respiratory alkalosis, alcoholism (alcohol withdrawal), diabetic ketoacidosis, malnutrition, obesity, and parenteral and enteral nutrition. In addition, HP may explain serious muscular, neurological, and haematological disorders and may cause peripheral neuropathy with paresthesias and metabolic encephalopathy, resulting in confusion and seizures. The neuropathy may be improved quickly after proper phosphate replacement. Phosphate depletion has been corrected using potassium-phosphate infusion, a treatment that can restore consciousness. In severe ataxia and tetra paresis, complete recovery can occur after adequate replacement of phosphate. Patients with multiple risk factors, often with a chronic disease and severe HP that contribute to phosphate depletion, are at risk for neurologic alterations. To predict both risk and optimal phosphate replenishment requires assessing the nutritional status and risk for re-feeding hypophosphatemia. The strategy for correcting HP depends on the severity of the underlying disease and the goal for re-establishing a phosphate balance to limit the consequences of phosphate depletion.
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PMID:Using phosphate supplementation to reverse hypophosphatemia and phosphate depletion in neurological disease and disturbance. 2590 52

Milk fever (MF) is a metabolic disease in dairy cows around parturition. The clinical lead sign is muscular paresis leading in severe cases to paralysis of the affected animal. Multiparturient animals of high performing dairy breeds are most likely to be affected and have a high probability of recurrence. An acute drop in blood calcium levels causes the disease when the demand for calcium at the onset of lactation exceeds the ability to replete blood calcium levels through mobilization from bone and intestinal uptake. With the understanding of the underlying mechanism, calcium supply management and vitamin D supplementation became prime candidates for MF prevention and therapy. Several strategies have been developed for MF prevention. Application of the active form of Vitamin D, 1,25(OH)2D3, was found to prevent MF effectively. In order to prevent a delayed hypocalcemia, which was occasionally seen after stopping the treatment with 1,25(OH)2D3, a new approach was chosen by applying Solanum glaucophyllum extract (SGE), which contains 1,25(OH)2D3-glycosides, as instant-release (irSGE) in combination with slow-release (srSGE) tablets. In a first study, non-lactating cows were treated with a single bolus of either synthetic 1,25(OH)2D3, irSGE, or srSGE and the results were compared to a control group without treatment. Blood serum levels of 1,25(OH)2D3 (1,25D), calcium (Ca), phosphate (P) and magnesium (Mg) were followed for 11days and the area under the curve (AUC) was calculated. Calcium and phosphate excretion in urine were determined during 15days. While serum concentration of 1,25(OH)2D3 was back to pre-treatment level in the irSGE, srSGE and 1,25(OH)2D3 treated group within 3days, calcium and phosphate levels remained elevated for up to 9days. AUC of serum 1,25(OH)2D3 was 2.89 (1,25D), 3.13 (irSGE) and 4.21 (srSGE) times higher than control. Serum calcium levels were 1.07* (for 1.25D); 1.08* (for irSGE) and 1.12* (for srSGE) times higher than control. Serum phosphate levels were 1.20* (for 1,25D); 1.30* (for irSGE) and 1.41* (for srSGE) times higher than control, with * p<0.05. In a second field study calving cows treated with one bolus containing ir- and sr- tablets of SGE were compared to an untreated control group and to a group treated with 4 boli of commercial calcium salts. As a result, calcium serum levels increased (+19% compared to baseline) around calving after treatment with the single bolus of SGE. The single bolus of SGE lead also to an increase of serum phosphate (+31% compared to baseline). These calcium and phosphate increases were statistically significant (p<0.001) 0-24h after calving compared to the control group and to the group treated with calcium salts. The sample size of the study was too small to draw a conclusion on the effect on MF prevention. In conclusion, application of a single bolus of a SGE extract lead to an increase of serum calcium and phosphate for up to 9days and may thus have the potential to prevent a hypocalcemia and -phosphatemia, an important cause for clinical milk fever.
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PMID:Effects of a sustained release formulation of 1,25-dihydroxyvitamin D3-glycosides for milk fever prevention on serum 1,25-dihydroxyvitamin D3, calcium and phosphorus in dairy cows. 2834 73

Tumour-induced osteomalacia (TIO), or oncogenic osteomalacia, is a paraneoplastic syndrome marked by hypophosphataemia, renal phosphate wasting, bone pain, weakness, and fractures. The syndrome has been reported with both benign and malignant tumours including parotid gland basal cell tumours, thyroid carcinomas, colon adenocarcinomas, and prostate cancer. Often, the syndrome is marked by an insidious course during which patients present with generalised bony pain and weakness, which do not resolve until the underlying tumour is identified and treated. We present a case of a patient with Parkinson's disease whose subacute weakness, lower extremity paresis, and renal phosphate wasting led to the synchronous diagnosis of metastatic prostate adenocarcinoma and TIO.
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PMID:Metastatic prostate cancer presenting as tumour-induced osteomalacia. 3131 44


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